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Published on: September 8, 2023
Coronavirus disease 2019 and the placenta: A literature review
Samwel R Gesaka1, Moses M Obimbo2, Anthony Wanyoro3
1Basic Clinical and Translational (BCT) Research Laboratory, University of Nairobi, Nairobi, Kenya.
Insights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect the placenta, affecting pregnancy. Viral entry mediators and pathogenesis mechanisms in placental tissues require further investigation.
Area of Science:
- Obstetrics and Gynecology
- Virology
- Pathology
Background:
- Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, impacts multiple organs.
- Understanding SARS-CoV-2's role in placental pathology is crucial due to the virus's novelty.
- Existing literature on placental SARS-CoV-2 infection requires synthesis.
Purpose of the Study:
- To review and evaluate the existing literature on SARS-CoV-2 in the placenta.
- To examine viral mediators, entry mechanisms, pathogenesis, detection, and pathology.
- To identify knowledge gaps regarding placental SARS-CoV-2 infection.
Main Methods:
- Systematic literature search yielding 96 eligible studies.
- Analysis of studies reporting on SARS-CoV-2 mediators, receptors, and factors in placental tissues.
- Review of methods for viral detection (in situ hybridization, PCR, etc.) and reported placental pathologies.
Main Results:
- Canonical mediators (ACE2, TMPRSS2) and other factors (SCARFs) are expressed in placental cells, influencing viral permissiveness.
- Viral RNA, proteins, and particles were detected primarily in syncytiotrophoblasts (STBs).
- Observed placental pathologies included maternal-fetal vascular malperfusion and inflammatory responses.
Conclusions:
- The placenta is predisposed to SARS-CoV-2 infection due to the expression of viral receptors and pathogenesis-related genes.
- SARS-CoV-2 infection can occur across all pregnancy trimesters, potentially exacerbated by pre-existing placental conditions.
- Further research is needed to fully elucidate the mechanisms of SARS-CoV-2 entry and pathogenesis in the placenta.
Abstract:
Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has been implicated in the clinical pathology of multiple organs and organ systems. Due to the novelty of the disease, there is a need to review emerging literature to understand the profile of SARS-CoV-2 in the placenta. This review sought to evaluate the literature on the mediators, mechanism of entry, pathogenesis, detection, and pathology of SARS-CoV-2 in the placenta. Systematic literature searches found 96 eligible studies. Our review revealed that SARS-CoV-2 canonical mediators, angiotensin-converting enzyme-2 (ACE2), and transmembrane serine protease-2 (TMPRSS2) are variably expressed in various placenta compartments, including the villous cytotrophoblasts, syncytiotrophoblasts (STBs), and extravillous trophoblasts (EVTs) throughout pregnancy. Placental SARS-CoV-2 and coronavirus-associated receptors and factors (SCARFs), including basigin (BSG/CD147), dipeptidyl peptidase-4 (DPP4/CD26), cathepsin B/L (CTL B/L), furin, interferon-induced transmembrane protein (IFITM1-3), and lymphocyte antigen 6E (LY6E) may increase or reduce the permissiveness of the placenta to SARS-CoV-2. EVTs express genes that code for proteins that may drive viral pathogenesis in the placenta. Viral RNA, proteins, and particles were detected primarily in the STBs by in situ hybridization, immunohistochemistry, electron microscopy, and polymerase chain reaction. Placental pathology in SARS-CoV-2-infected placentas included maternal and fetal vascular malperfusion and a generally nonspecific inflammatory-immune response. The localization of SARS-CoV-2 receptors, proteases, and genes involved in coding proteins that drive viral pathogenesis in the placenta predisposes the placenta to SARS-CoV-2 infection variably in all pregnancy trimesters, with antecedent placental pathology. There is a need for further studies to explicate the mechanism of entry and pathogenesis of SARS-CoV-2 in the placenta.
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